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Prostate. 2008 Jan 1;68(1):72-7.

Involvement of decreased Galectin-3 expression in the pathogenesis and progression of prostate cancer.

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Department of Urology, Eberhard Karls University Tübingen, Germany.



Altered expression or loss of function of Galectin-3 (Gal-3) was suggested to be involved in the pathogenesis and progression of various human cancer entities. The aim of the present study is to determine the expression of Gal-3 in prostate tissue emerging from a benign to a malignant, in the beginning hormone-sensitive and finally hormone-refractory status to further elucidate the role of this carbohydrate-binding protein for the pathogenesis and/or progression of malignant prostatic disease.


Five hundred and eighty three tissue samples from malignant, tumor adjacent benign, and histologically benign intra-prostatic areas, retrieved out of 25 whole mounted prostate cancer (CaP) specimens and additional 95 samples of hormone-refractory CaP, were processed to tissue microarrays. Immunohistochemical Gal-3 expression was correlated with clinicopathological parameters among the different tissue entities.


Gal-3 expression was significantly decreased in the hormone-sensitive CaP specimens when compared with the respective benign tissue either localized far distant from the malignant lesion (P < 0.0001, Wilcoxon test) or directly neighboring the primary tumor (P < 0.0001). The staining reaction in the benign tissue areas directly neighboring the primary cancerous lesions differed significantly from the benign glands localized distant from the primary tumors (P < 0.001). A statistically highly significant, almost complete loss of Gal-3 was observed in the hormone-refractory when compared with the hormone-sensitive tumors (P < 0.0001; mean staining score: 27.7% vs. 8.5%).


The present investigation clearly indicates decreased expression of Gal-3 to be substantially involved in the pathogenesis and further progression of CaP from benign prostate glands to a finally hormone-refractory malignant disease.

[Indexed for MEDLINE]

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